44 Paul Fourman and Patricia M. Leeson 



this amount routinely. Gordon and Goldner gave one of their 

 two patients 8-24 litres in 24 hours and even this was not 

 enough to bring down his plasma [Na] to normal. As long as 

 the plasma [Na] remains high there can be no risk of water 

 intoxication. 



Other forms of hypernatraemia. 



It is possible to produce hypernatraemia by giving an 

 excess of salt (McCance, 1956), though more usually this 

 produces an isotonic expansion of the extracellular fluid with 

 oedema. 



The homeostatic mechanisms may be so adjusted as to 

 maintain the plasma [Na] at a high level. In experimental 

 potassium deficiency the plasma [Na] was over 150 m-equiv./L, 

 although the absorption of sodium was small and the intake 

 of water as much as eight litres a day in one subject (Fourman, 

 1954). Hypernatraemia is often a feature of aldosteronism 

 (Conn, 1956) but whether or not this is the result of the 

 associated potassium deficiency cannot be stated. Recently 

 Zilva and Harris- Jones (1957) have discussed the possibility 

 of excessive adrenocortical activity producing hypernatraemia 

 by a shift of sodium from cells to ECF. 



Hyponatraemia 



We may arbitrarily define hyponatraemia as a plasma [Na] 

 lower than 180 m-equiv./l. It is obvious the concentration of 

 sodium in the plasma may fall because of a reduction in the 

 total amount of sodium in the ECF or because of an increase 

 in the amount of water. 



Salt deficiency 



A reduction of the total amount of sodium in the ECF is 

 the result of sodium deficiency. 



We have already emphasized that the clinical effects of 

 sodium deficiency are easily recognizable. Lack of salt is un- 

 likely to arise unless, through sweating, vomiting, diarrhoea 

 or fistulous discharge, sodium is lost from the body, because 



